Foods to Avoid to Help Prevent Diabetes

Oct 24 Foods to Avoid copy.jpeg

We've known that being overweight and obese are important risk factors for type 2 diabetes, but, until recently, not much attention has been paid to the role of specific foods. I discuss this issue in my video, Why Is Meat a Risk Factor for Diabetes?

A 2013 meta-analysis of all the cohorts looking at the connection between meat and diabetes found a significantly higher risk associated with total meat consumption--especially consumption of processed meat, particularly poultry. But why? There's a whole list of potential culprits in meat: saturated fat, animal fat, trans fats naturally found in meat, cholesterol, or animal protein. It could be the heme iron found in meat, which can lead to free radicals and iron-induced oxidative stress that may lead to chronic inflammation and type 2 diabetes, or advanced glycation end (AGE) products, which promote oxidative stress and inflammation. Food analyses show that the highest levels of these so-called glycotoxins are found in meat--particularly roasted, fried, or broiled meat, though any foods from animal sources (and even high fat and protein plant foods such as nuts) exposed to high dry temperatures can be potent sources of these pro-oxidant chemicals.

In another study, researchers fed diabetics glycotoxin-packed foods, like chicken, fish, and eggs, and their inflammatory markers--tumor necrosis factor, C-reactive protein, and vascular adhesion molecules--shot up. "Thus, in diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury." The good news is that restriction of these kinds of foods may suppress these inflammatory effects. Appropriate measures to limit AGE intake, such as eliminating meat or using only steaming and boiling as methods for cooking it, "may greatly reduce the already heavy burden of these toxins in the diabetic patient." These glycotoxins may be the missing link between the increased consumption of animal fat and meats and the development of type 2 diabetes.

Since the 2013 meta-analysis was published, another study came out in which approximately 17,000 people were followed for about a dozen years. Researchers found an 8% increased risk for every 50 grams of daily meat consumption. Just one quarter of a chicken breast's worth of meat for the entire day may significantly increase the risk of diabetes. Yes, we know there are many possible culprits: the glycotoxins or trans fat in meat, saturated fat, or the heme iron (which could actually promote the formation of carcinogens called nitrosamines, though they could also just be produced in the cooking process itself). However, we did learn something new: There also appears to be a greater incidence of diabetes among those who handle meat for a living. Maybe there are some diabetes-causing zoonotic infectious agents--such as viruses--present in fresh cuts of meat, including poultry.

A "crucial factor underlying the diabetes epidemic" may be the overstimulation of the aging enzyme TOR pathway by excess food consumption--but not by the consumption of just any food: Animal proteins not only stimulate the cancer-promoting hormone insulin growth factor-1 but also provide high amounts of leucine, which stimulates TOR activation and appears to contribute to the burning out of the insulin-producing beta cells in the pancreas, contributing to type 2 diabetes. So, it's not just the high fat and added sugars that are implicated; critical attention must be paid to the daily intake of animal proteins as well.

According to a study, "[i]n general, lower leucine levels are only reached by restriction of animal proteins." To reach the leucine intake provided by dairy or meat, we'd have to eat 9 pounds of cabbage or 100 apples to take an extreme example. That just exemplifies the extreme differences in leucine amounts provided by a more standard diet in comparison with a more plant-based diet.

I reviewed the role endocrine-disrupting industrial pollutants in the food supply may play in a three-part video series: Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat. Clearly, the standard America diet and lifestyle contribute to the epidemic of diabetes and obesity, but the contribution of these industrial pollutants can no longer be ignored. We now have experimental evidence that exposure to industrial toxins alone induces weight gain and insulin resistance, and, therefore, may be an underappreciated cause of obesity and diabetes. Consider what's happening to our infants: Obesity in a six-month-old is obviously not related to diet or lack of exercise. They're now exposed to hundreds of chemicals from their moms, straight through the umbilical cord, some of which may be obesogenic (that is, obesity-generating).

The millions of pounds of chemicals and heavy metals released every year into our environment should make us all stop and think about how we live and the choices we make every day in the foods we eat. A 2014 review of the evidence on pollutants and diabetes noted that we can be exposed through toxic spills, but "most of the human exposure nowadays is from the ingestion of contaminated food as a result of bioaccumulation up the food chain. The main source (around 95%) of [persistent pollutant] intake is through dietary intake of animal fats."


For more on the information mentioned here, see the following videos that take a closer look at these major topics:

AGEs: Glycotoxins, Avoiding a Sugary Grave, and Reducing Glycotoxin Intake to Prevent Alzheimer's.

TOR: Why Do We Age?, Caloric Restriction vs. Animal Protein Restriction, Prevent Cancer From Going on TOR, and Saving Lives By Treating Acne With Diet

Viruses: Infectobesity: Adenovirus 36 and Childhood Obesity

Poultry workers: Poultry Exposure and Neurological Disease, Poultry Exposure Tied to Liver and Pancreatic Cancer, and Eating Outside Our Kingdom

Industrial pollutants: Obesity-Causing Pollutants in Food, Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat

The link between meat and diabetes may also be due to a lack of sufficient protective components of plants in the diet, which is discussed in my videos How May Plants Protect Against Diabetes?, Plant-Based Diets for Diabetes, Plant-Based Diets and Diabetes, and How Not to Die from Diabetes.

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image credit: TV Brasil EBC via Flickr. This image has been modified.

Original Link

Foods to Avoid to Help Prevent Diabetes

Oct 24 Foods to Avoid copy.jpeg

We've known that being overweight and obese are important risk factors for type 2 diabetes, but, until recently, not much attention has been paid to the role of specific foods. I discuss this issue in my video, Why Is Meat a Risk Factor for Diabetes?

A 2013 meta-analysis of all the cohorts looking at the connection between meat and diabetes found a significantly higher risk associated with total meat consumption--especially consumption of processed meat, particularly poultry. But why? There's a whole list of potential culprits in meat: saturated fat, animal fat, trans fats naturally found in meat, cholesterol, or animal protein. It could be the heme iron found in meat, which can lead to free radicals and iron-induced oxidative stress that may lead to chronic inflammation and type 2 diabetes, or advanced glycation end (AGE) products, which promote oxidative stress and inflammation. Food analyses show that the highest levels of these so-called glycotoxins are found in meat--particularly roasted, fried, or broiled meat, though any foods from animal sources (and even high fat and protein plant foods such as nuts) exposed to high dry temperatures can be potent sources of these pro-oxidant chemicals.

In another study, researchers fed diabetics glycotoxin-packed foods, like chicken, fish, and eggs, and their inflammatory markers--tumor necrosis factor, C-reactive protein, and vascular adhesion molecules--shot up. "Thus, in diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury." The good news is that restriction of these kinds of foods may suppress these inflammatory effects. Appropriate measures to limit AGE intake, such as eliminating meat or using only steaming and boiling as methods for cooking it, "may greatly reduce the already heavy burden of these toxins in the diabetic patient." These glycotoxins may be the missing link between the increased consumption of animal fat and meats and the development of type 2 diabetes.

Since the 2013 meta-analysis was published, another study came out in which approximately 17,000 people were followed for about a dozen years. Researchers found an 8% increased risk for every 50 grams of daily meat consumption. Just one quarter of a chicken breast's worth of meat for the entire day may significantly increase the risk of diabetes. Yes, we know there are many possible culprits: the glycotoxins or trans fat in meat, saturated fat, or the heme iron (which could actually promote the formation of carcinogens called nitrosamines, though they could also just be produced in the cooking process itself). However, we did learn something new: There also appears to be a greater incidence of diabetes among those who handle meat for a living. Maybe there are some diabetes-causing zoonotic infectious agents--such as viruses--present in fresh cuts of meat, including poultry.

A "crucial factor underlying the diabetes epidemic" may be the overstimulation of the aging enzyme TOR pathway by excess food consumption--but not by the consumption of just any food: Animal proteins not only stimulate the cancer-promoting hormone insulin growth factor-1 but also provide high amounts of leucine, which stimulates TOR activation and appears to contribute to the burning out of the insulin-producing beta cells in the pancreas, contributing to type 2 diabetes. So, it's not just the high fat and added sugars that are implicated; critical attention must be paid to the daily intake of animal proteins as well.

According to a study, "[i]n general, lower leucine levels are only reached by restriction of animal proteins." To reach the leucine intake provided by dairy or meat, we'd have to eat 9 pounds of cabbage or 100 apples to take an extreme example. That just exemplifies the extreme differences in leucine amounts provided by a more standard diet in comparison with a more plant-based diet.

I reviewed the role endocrine-disrupting industrial pollutants in the food supply may play in a three-part video series: Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat. Clearly, the standard America diet and lifestyle contribute to the epidemic of diabetes and obesity, but the contribution of these industrial pollutants can no longer be ignored. We now have experimental evidence that exposure to industrial toxins alone induces weight gain and insulin resistance, and, therefore, may be an underappreciated cause of obesity and diabetes. Consider what's happening to our infants: Obesity in a six-month-old is obviously not related to diet or lack of exercise. They're now exposed to hundreds of chemicals from their moms, straight through the umbilical cord, some of which may be obesogenic (that is, obesity-generating).

The millions of pounds of chemicals and heavy metals released every year into our environment should make us all stop and think about how we live and the choices we make every day in the foods we eat. A 2014 review of the evidence on pollutants and diabetes noted that we can be exposed through toxic spills, but "most of the human exposure nowadays is from the ingestion of contaminated food as a result of bioaccumulation up the food chain. The main source (around 95%) of [persistent pollutant] intake is through dietary intake of animal fats."


For more on the information mentioned here, see the following videos that take a closer look at these major topics:

AGEs: Glycotoxins, Avoiding a Sugary Grave, and Reducing Glycotoxin Intake to Prevent Alzheimer's.

TOR: Why Do We Age?, Caloric Restriction vs. Animal Protein Restriction, Prevent Cancer From Going on TOR, and Saving Lives By Treating Acne With Diet

Viruses: Infectobesity: Adenovirus 36 and Childhood Obesity

Poultry workers: Poultry Exposure and Neurological Disease, Poultry Exposure Tied to Liver and Pancreatic Cancer, and Eating Outside Our Kingdom

Industrial pollutants: Obesity-Causing Pollutants in Food, Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat

The link between meat and diabetes may also be due to a lack of sufficient protective components of plants in the diet, which is discussed in my videos How May Plants Protect Against Diabetes?, Plant-Based Diets for Diabetes, Plant-Based Diets and Diabetes, and How Not to Die from Diabetes.

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image credit: TV Brasil EBC via Flickr. This image has been modified.

Original Link

Comparing Pollutant Levels Between Different Diets

Comparing Pollutant Levels Between Different Diets.jpeg

The results of the CHAMACOS (Center for the Health Assessment of Mothers and Children of Salinas) study were published recently. This study of a California birth cohort investigated the relationship between exposure to flame retardant chemical pollutants in pregnancy and childhood, and subsequent neurobehavioral development. Why California? Because California children's exposures to these endocrine disruptors and neurotoxins are among the highest in the world.

What did they find? The researchers concluded that both prenatal and childhood exposures to these chemicals "were associated with poorer attention, fine motor coordination, and cognition" (particularly verbal comprehension) by the time the children reached school age. "This study, the largest to date, contributes to growing evidence suggesting that PBDEs [polybrominated diphenyl ethers, flame retardant chemicals] have adverse impacts on child neurobehavioral development." The effects may extend into adolescence, again affecting motor function as well as thyroid gland function. The effect on our thyroid glands may even extend into adulthood.

These chemicals get into moms, then into the amniotic fluid, and then into the breast milk. The more that's in the milk, the worse the infants' mental development may be. Breast milk is still best, but how did these women get exposed in the first place?

The question has been: Are we exposed mostly from diet or dust? Researchers in Boston collected breast milk samples from 46 first-time moms, vacuumed up samples of dust from their homes, and questioned them about their diets. The researchers found that both were likely to blame. Diet-wise, a number of animal products were implicated. This is consistent with what's been found worldwide. For example, in Europe, these flame retardant chemical pollutants are found mostly in meat, including fish, and other animal products. It's similar to what we see with dioxins--they are mostly found in fish and other fatty foods, with a plant-based diet offering the lowest exposure.

If that's the case, do vegetarians have lower levels of flame retardant chemical pollutants circulating in their bloodstreams? Yes. Vegetarians may have about 25% lower levels. Poultry appears to be the largest contributor of PBDEs. USDA researchers compared the levels in different meats, and the highest levels of these pollutants were found in chicken and turkey, with less in pork and even less in beef. California poultry had the highest, consistent with strict furniture flammability codes. But it's not like chickens are pecking at the sofa. Chickens and turkeys may be exposed indirectly through the application of sewer sludge to fields where feed crops are raised, contamination of water supplies, the use of flame-retarded materials in poultry housing, or the inadvertent incorporation of fire-retardant material into the birds' bedding or feed ingredients.

Fish have been shown to have the highest levels overall, but Americans don't eat a lot of fish so they don't contribute as much to the total body burden in the United States. Researchers have compared the level of PBDEs found in meat-eaters and vegetarians. The amount found in the bloodstream of vegetarians is noticeably lower, as you can see in my video Flame Retardant Pollutants and Child Development. Just to give you a sense of the contribution of chicken, higher than average poultry eaters have higher levels than omnivores as a whole, and lower than average poultry eaters have levels lower than omnivores.

What are the PBDE levels in vegans? We know the intake of many other classes of pollutants is almost exclusively from the ingestion of animal fats in the diet. What if we take them all out of the diet? It works for dioxins. Vegan dioxin levels appear markedly lower than the general population. What about for the flame retardant chemicals? Vegans have levels lower than vegetarians, with those who've been vegan around 20 years having even lower concentrations. This tendency for chemical levels to decline the longer one eats plant-based suggests that food of animal origin contributes substantially. But note that levels never get down to zero, so diet is not the only source.

The USDA researchers note that there are currently no regulatory limits on the amount of flame retardant chemical contamination in U.S. foods, "but reducing the levels of unnecessary, persistent, toxic compounds in our diet is certainly desirable."

I've previously talked about this class of chemicals in Food Sources of Flame Retardant Chemicals. The same foods seem to accumulate a variety of pollutants:

Many of these chemicals have hormone- or endocrine-disrupting effects. See, for example:

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Mitchell Haindfield / Flickr. This image has been modified.

Original Link

Comparing Pollutant Levels Between Different Diets

Comparing Pollutant Levels Between Different Diets.jpeg

The results of the CHAMACOS (Center for the Health Assessment of Mothers and Children of Salinas) study were published recently. This study of a California birth cohort investigated the relationship between exposure to flame retardant chemical pollutants in pregnancy and childhood, and subsequent neurobehavioral development. Why California? Because California children's exposures to these endocrine disruptors and neurotoxins are among the highest in the world.

What did they find? The researchers concluded that both prenatal and childhood exposures to these chemicals "were associated with poorer attention, fine motor coordination, and cognition" (particularly verbal comprehension) by the time the children reached school age. "This study, the largest to date, contributes to growing evidence suggesting that PBDEs [polybrominated diphenyl ethers, flame retardant chemicals] have adverse impacts on child neurobehavioral development." The effects may extend into adolescence, again affecting motor function as well as thyroid gland function. The effect on our thyroid glands may even extend into adulthood.

These chemicals get into moms, then into the amniotic fluid, and then into the breast milk. The more that's in the milk, the worse the infants' mental development may be. Breast milk is still best, but how did these women get exposed in the first place?

The question has been: Are we exposed mostly from diet or dust? Researchers in Boston collected breast milk samples from 46 first-time moms, vacuumed up samples of dust from their homes, and questioned them about their diets. The researchers found that both were likely to blame. Diet-wise, a number of animal products were implicated. This is consistent with what's been found worldwide. For example, in Europe, these flame retardant chemical pollutants are found mostly in meat, including fish, and other animal products. It's similar to what we see with dioxins--they are mostly found in fish and other fatty foods, with a plant-based diet offering the lowest exposure.

If that's the case, do vegetarians have lower levels of flame retardant chemical pollutants circulating in their bloodstreams? Yes. Vegetarians may have about 25% lower levels. Poultry appears to be the largest contributor of PBDEs. USDA researchers compared the levels in different meats, and the highest levels of these pollutants were found in chicken and turkey, with less in pork and even less in beef. California poultry had the highest, consistent with strict furniture flammability codes. But it's not like chickens are pecking at the sofa. Chickens and turkeys may be exposed indirectly through the application of sewer sludge to fields where feed crops are raised, contamination of water supplies, the use of flame-retarded materials in poultry housing, or the inadvertent incorporation of fire-retardant material into the birds' bedding or feed ingredients.

Fish have been shown to have the highest levels overall, but Americans don't eat a lot of fish so they don't contribute as much to the total body burden in the United States. Researchers have compared the level of PBDEs found in meat-eaters and vegetarians. The amount found in the bloodstream of vegetarians is noticeably lower, as you can see in my video Flame Retardant Pollutants and Child Development. Just to give you a sense of the contribution of chicken, higher than average poultry eaters have higher levels than omnivores as a whole, and lower than average poultry eaters have levels lower than omnivores.

What are the PBDE levels in vegans? We know the intake of many other classes of pollutants is almost exclusively from the ingestion of animal fats in the diet. What if we take them all out of the diet? It works for dioxins. Vegan dioxin levels appear markedly lower than the general population. What about for the flame retardant chemicals? Vegans have levels lower than vegetarians, with those who've been vegan around 20 years having even lower concentrations. This tendency for chemical levels to decline the longer one eats plant-based suggests that food of animal origin contributes substantially. But note that levels never get down to zero, so diet is not the only source.

The USDA researchers note that there are currently no regulatory limits on the amount of flame retardant chemical contamination in U.S. foods, "but reducing the levels of unnecessary, persistent, toxic compounds in our diet is certainly desirable."

I've previously talked about this class of chemicals in Food Sources of Flame Retardant Chemicals. The same foods seem to accumulate a variety of pollutants:

Many of these chemicals have hormone- or endocrine-disrupting effects. See, for example:

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Mitchell Haindfield / Flickr. This image has been modified.

Original Link

How Milk May Contribute to Childhood Obesity

How Milk May Contribute to Childhood Obesity.jpeg

We've known that breastfed infants may be protected against obesity later in life for more than 30 years, but why? It may be the formula. Giving infants formula based on cow's milk presents an unusual situation. Cow's milk is designed to put nearly two pounds a day onto a growing calf, 40 times the growth rate of human infants (see Formula for Childhood Obesity).

The perfect food for humans, finely tuned over millions of years, is human breast milk. Remarkably, among all mammalian species, the protein content of human milk is the lowest. The excessive protein content of cow's milk-based formula is thought to be what may be what sets the child up for obesity later in life.

And then, instead of being weaned, we continue to drink milk. The question thus arises as to whether consumption of a growth-promoting substance from another species throughout childhood fundamentally alters processes of human growth and maturation. A study out of Indiana University, for example, found evidence that greater milk intake is associated with an increased risk of premature puberty; girls drinking a lot of milk started to get their periods earlier. Thus, cross-species milk consumption and ingestion into childhood may trigger unintended consequences.

Only human milk allows appropriate metabolic programming and protects against diseases of civilization in later life, whereas consumption of cow's milk and dairy products during adolescence and adulthood is an evolutionarily novel behavior that may have long-term adverse effects on human health.

Teens exposed to dairy proteins such as casein, skim milk, or whey, experienced a significant increase in BMI and waist circumference compared to a control group. In contrast, not a single study funded by the dairy industry found a result unfavorable to milk.

The head of the Obesity Prevention Center at Boston Children's Hospital and the chair of Harvard's nutrition department wrote an editorial recently to the AMA's Pediatrics journal questioning the role of cow's milk in human nutrition. They stated the obvious: humans have no requirement for other animal's milk; in fact, dairy may play a role in certain cancers due to the high levels of reproductive hormones in the U.S. milk supply.


So what's The Best Baby Formula? Click on the link and find out!

More on dairy and infancy:

And in childhood: Childhood Constipation and Cow's Milk and Treating Infant Colic by Changing Mom's Diet

In adolescence: Saving Lives By Treating Acne With Diet

Before conception: Dairy Estrogen and Male Fertility

During pregnancy: Why Do Vegan Women Have 5x Fewer Twins?

And in adulthood:

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Sergey Novikov © 123RF.com. This image has been modified.

Original Link

How Milk May Contribute to Childhood Obesity

How Milk May Contribute to Childhood Obesity.jpeg

We've known that breastfed infants may be protected against obesity later in life for more than 30 years, but why? It may be the formula. Giving infants formula based on cow's milk presents an unusual situation. Cow's milk is designed to put nearly two pounds a day onto a growing calf, 40 times the growth rate of human infants (see Formula for Childhood Obesity).

The perfect food for humans, finely tuned over millions of years, is human breast milk. Remarkably, among all mammalian species, the protein content of human milk is the lowest. The excessive protein content of cow's milk-based formula is thought to be what may be what sets the child up for obesity later in life.

And then, instead of being weaned, we continue to drink milk. The question thus arises as to whether consumption of a growth-promoting substance from another species throughout childhood fundamentally alters processes of human growth and maturation. A study out of Indiana University, for example, found evidence that greater milk intake is associated with an increased risk of premature puberty; girls drinking a lot of milk started to get their periods earlier. Thus, cross-species milk consumption and ingestion into childhood may trigger unintended consequences.

Only human milk allows appropriate metabolic programming and protects against diseases of civilization in later life, whereas consumption of cow's milk and dairy products during adolescence and adulthood is an evolutionarily novel behavior that may have long-term adverse effects on human health.

Teens exposed to dairy proteins such as casein, skim milk, or whey, experienced a significant increase in BMI and waist circumference compared to a control group. In contrast, not a single study funded by the dairy industry found a result unfavorable to milk.

The head of the Obesity Prevention Center at Boston Children's Hospital and the chair of Harvard's nutrition department wrote an editorial recently to the AMA's Pediatrics journal questioning the role of cow's milk in human nutrition. They stated the obvious: humans have no requirement for other animal's milk; in fact, dairy may play a role in certain cancers due to the high levels of reproductive hormones in the U.S. milk supply.


So what's The Best Baby Formula? Click on the link and find out!

More on dairy and infancy:

And in childhood: Childhood Constipation and Cow's Milk and Treating Infant Colic by Changing Mom's Diet

In adolescence: Saving Lives By Treating Acne With Diet

Before conception: Dairy Estrogen and Male Fertility

During pregnancy: Why Do Vegan Women Have 5x Fewer Twins?

And in adulthood:

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Sergey Novikov © 123RF.com. This image has been modified.

Original Link

Evidence-Based Nutrition

NF-Jan12 Evidence-Based Medicine or Evidence-Biased?.jpg

Dr. Esselstyn's landmark study, demonstrating that even advanced triple vessel coronary artery disease could be reversed with a plant-based diet, has been criticized for being such a small study. But the reason we're used to seeing large studies is that they typically show such small effects. Drug manufacturers may need to study 7,000 people in order to show a barely statistically significant 15% drop in ischemic events in a subsample of patients. Esselstyn achieved a 100% drop in those who stuck to his diet, all the more compelling considering that those 18 participants experienced 49 coronary events (like heart attacks) in the eight years before they went on the diet. These patients were the sickest of the sick, most of whom having already failed surgical intervention. When the effects are so dramatic, how many people do you need?

Before 1885, a symptomatic rabies infection was a death sentence, until little Joseph Meister became the first to receive Pasteur's experimental rabies vaccine. The results of this and one other case were so dramatic compared with previous experience that the new treatment was accepted with a sample size of two. That is, the results were so compelling that no randomized controlled trial was necessary. Having been infected by a rabid dog, would you be willing to participate in a randomized controlled trial, when being in the control group had a certainty of a ''most awful death''? Sadly, such a question is not entirely rhetorical.

In the 1970's, a revolutionary treatment for babies with immature lungs called "extracorporeal membranous oxygenation" (ECMO), transformed immature lung mortality from 80% dead to 80% alive nearly overnight. The standard therapy caused damage to infants' lungs and was a major cause of morbidity and mortality in infants. ECMO is much gentler on babies' lungs, "providing life support while allowing the lungs to 'rest.'"

Despite their dramatic success, the researchers who developed ECMO felt forced to perform a randomized controlled trial. They didn't want to; they knew they'd be condemning babies to death. They felt compelled to perform such a trial because their claim that ECMO worked would, they judged, carry little weight amongst their medical colleagues unless supported by a randomized controlled trial. Therefore, at Harvard's Children's Hospital, 39 infants were randomized to either get ECMO or conventional medical therapy. The researchers decided ahead of time to stop the trial after the 4th death so as not to kill too many babies. And that's what they did. The study was halted after the fourth conventional medical therapy death, at which point nine out of nine ECMO babies had survived. Imagine being the parent to one of those four children.

Similarly, imagine being the child of a parent who died other conventional medical or surgical therapy for heart disease.

In her paper "How evidence-based medicine biases physicians against nutrition," Laurie Endicott Thomas reminds us that medical students in the United States are taught very little about nutrition (See Evidence-Based Medicine or Evidence-Biased?). Worse yet, according to Thomas, their training actually biases them against the studies that show the power of dietary approaches to managing disease by encouraging them to ignore any information that does not come from a double-blind, randomized controlled trial. Yet humans cannot be blinded to a dietary intervention--we tend to notice what we're eating--and, as a result, physicians are biased in favor of drug treatments and against dietary interventions for the management of chronic disease.

Evidence-based medicine is a good thing. However, Thomas points out that the medical profession may be focusing too much on one type of evidence to the exclusion of all others. Unfortunately, this approach can easily degenerate into "ignoring-most-of-the-truly-important-evidence" based medicine.

Heart disease is a perfect example. On healthy enough plant based diets, our number one cause of death may simply cease to exist. The Cornell-Oxford-China Study showed that even small amounts of animal-based food was associated with a small, but measurable increase in the risk of some chronic diseases. In other words, "the causal relationship between dietary patterns and coronary artery disease was already well established before Dean Ornish and Caldwell Esselstyn undertook their clinical studies." The value of their studies was not so much in providing evidence that such a dietary change would be effective, but in showing that "physicians can persuade their patients to make such changes," and in "providing interesting data on the speed and magnitude of the change in severe atherosclerotic lesions as a result of dietary therapy."

Therefore, any complaints that these studies were small or unblinded are simply irrelevant. Because the evidence of the role of diet in causing atherosclerosis is already so overwhelming, "assigning a patient to a control group eating the standard American diet could be considered a violation of research ethics."

Evidence of the value of plant-based diets for managing chronic disease has been available in the medical literature for decades. Walter Kempner at Duke University, John McDougall, the Physician's Committee for Responsible Medicine, Nathan Pritikin, and Denis Burkitt all warned us that the standard Western diet is the standard cause of death and disability in the Western world. Yet physicians, especially in the US, are still busily manning the ambulances at the bottom of the cliff instead of building fences at the top.

If you're not familiar with Dr. Esselstyn's work, I touch on it in:

Sadly, medical students learn little about these powerful tools:

If you haven't heard of Pritikin, I introduce him here: Engineering a Cure

An intro to Dr. Ornish: Convergence of Evidence

Dr. Burkitt: Dr. Burkitt's F-Word Diet

The Cornell-Oxford-China Study: China Study on Sudden Cardiac Death

Dr. Walter Kempner: Kempner Rice Diet: Whipping Us Into Shape

-Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death, More Than an Apple a Day, From Table to Able, and Food as Medicine.

Image Credit: clement127 / Flickr

Original Link

The Dietary Link Between Acne and Cancer

NF-Jan7 Saving Lives By Treating Acne With Diet.jpg

Acne is an epidemic skin disease of industrialized countries, reaching prevalence rates of over 85 percent of teenagers. In nearly half of American men and women, acne even continues after adolescence and into the third decade of life.

Acne is considered a disease of Western civilization, as in places like Okinawa, Japan, acne is rare or even nonexistent. So acne is not some "physiological" phenomenon of puberty, but may represent "a visible risk indicator pointing to aberrant nutrient signaling promoting chronic epidemic diseases of civilization," according to a group of German researchers (See Saving Lives By Treating Acne With Diet). What they mean is that the dairy, junk foods, meat, and egg proteins in Western diets all conspire to raise the activity of the enzyme TOR, contributing to acne and obesity. Therefore, using diet to suppress TOR may not only improve acne, but may also prevent the march to more serious chronic TOR-driven diseases of civilization. The excessive TOR stimulation induced by the standard American diet may initially manifest as premature puberty and acne, but then may later contribute to obesity, diabetes, cancer and Alzheimer's.

A lot of this research is relatively new. Until recently, for example, only a weak association had been accepted for the role of milk and dairy products in acne formation. However, there is now substantial evidence supporting the effects of milk and dairy products as enhancers of acne aggravation. Milk is not just food, but appears to represent a most sophisticated hormone signaling system activating TOR, which is of critical concern given that TOR is recognized as the fundamental driving force for a number of serious chronic diseases.

If milk is naturally supposed to stimulate TOR, why the problem? Because we're drinking milk from the wrong species. Cow's milk is designed for calves. Baby cows grow nearly 40 times faster than human infants. Cow's milk has three times more leucine, the primary activator of TOR, than breast milk, so cow's milk may over-stimulate TOR when consumed by humans. It's like giving donkey milk to rats--it doesn't make sense. Furthermore, milk is for babies, so the continued consumption of any kind of milk during adolescence and adulthood is something that never really happened naturally and may have long-term adverse effects on human health.

In this regard, it's kind of frightening to realize that more than 85 percent of teens in Western countries exhibit acne; it implies that the "majority of our population is living with over-activated TOR signaling, a major disease-causing factor, which may pave the way for the development of other more serious diseases." A history of acne has been associated with breast cancer risk in women, for example, and prostate cancer in men.

So early dietary counseling of teenage acne patients is thus a great opportunity for dermatologists, who will not only help to improve acne but may reduce the long-term adverse effects of Western diet on more serious TOR-driven diseases. So just like urologists use erectile dysfunction as an opportunity to save lives by putting people on heart-healthy diets, dermatologists can use acne as a way to save lives by putting people on a cancer prevention diet.

How do you turn acne on and off via dietary manipulation of TOR? A "comprehensive dietary strategy to treat acne can only be achieved by higher consumption of vegetables and fruit and reduction of animal-derived food" given preliminary evidence for the effectiveness of natural plant-derived TOR inhibitors in the treatment of acne.

TOR is considered the engine-of-aging enzyme detailed in Why Do We Age? and Caloric Restriction vs. Animal Protein Restriction, as well as my video Prevent Cancer From Going on TOR.

I've touched on this topic before in Acne and Cancer and covered acne and dairy in:

Urologists saving the lives of men is detailed in Survival of the Firmest: Erectile Dysfunction and Death and 50 Shades of Greens.

What else are Okinawans doing right? See The Okinawa Diet: Living to 100.

-Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death, More Than an Apple a Day, From Table to Able, and Food as Medicine.

Image Credit: coniferconfier / Flickr

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How to Suppress the Aging Enzyme TOR

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Over the last decade, more than 5,000 papers have been published about TOR, an engine-of-aging enzyme inhibited by the drug rapamycin. (What is TOR? Check out my videos Why Do We Age? and Caloric Restriction vs. Animal Protein Restriction.) Rapamycin has been used experimentally to extend lifespan, but is already in use clinically to prevent the rejection of kidney transplants. Patients who received rapamycin due to renal transplantation had a peculiar "side effect," a decrease in cancer incidence. In a set of 15 patients who had biopsy proven Kaposi's sarcoma (a cancer that often affects the skin), all cutaneous sarcoma lesions disappeared in all patients within three months after starting rapamycin therapy.

TOR functions as a master regulator of cellular growth and proliferation. For example, TOR is upregulated in nearly 100% of advanced human prostate cancers (See Prevent Cancer From Going on TOR). So, reductions in cancerous lesions after rapamycin therapy make sense. TOR may also be why dairy consumption has been found to be a major dietary risk factor for prostate cancer. We used to think it was just the hormones in milk, but maybe prostate cancer initiation and progression is also promoted by cow's milk stimulation of TOR.

Our understanding of mammalian milk has changed from a simple food to a "species-specific endocrine signaling system," which activates TOR, promoting cell growth and proliferation and suppressing our body's internal housecleaning mechanisms. Normally, milk-mediated TOR stimulation is restricted only to infancy where we really need that constant signal to our cells to grow and divide. So from an evolutionary perspective, "the persistent 'abuse' of the growth-promoting signaling system of cow's milk by drinking milk over our entire life span may maintain the most important hallmark of cancer biology, sustained proliferative signaling."

TOR appears to play a role in breast cancer, too. Higher TOR expression has been noted in breast cancer tumors, associated with more aggressive disease, and lower survival rate among breast cancer patients. Altered TOR expression could explain why women hospitalized for anorexia may end up with only half the risk of breast cancer. Severe caloric restriction in humans may confer protection from invasive breast cancer by suppressing TOR activation.

We don't have to starve ourselves to suppress TOR; just reducing animal protein intake can attenuate overall TOR activity. Moreover, diets emphasizing plants, especially cruciferous vegetables, have both decreased TOR activation from animal proteins and provide natural plant-derived inhibitors of TOR found in broccoli, green tea, soy, turmeric, and grapes, along with other fruits and vegetables such as onions, strawberries, blueberries, mangoes and the skin of cucumbers.

The downregulation of TOR may be one reason why plant-based in general are associated with lower risk for many cancers. "Are we finally on the threshold of being able to fundamentally alter human aging and age-related disease?" asks researchers in the journal Nature. Only time will tell, but if the pace and direction of recent progress are any indication, the next 5,000 studies on TOR should prove very interesting indeed.

More on dairy and prostate cancer in Prostate Cancer and Organic Milk vs. Almond Milk.

This story continues in my video: Saving Lives By Treating Acne With Diet.

-Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death, More Than an Apple a Day, From Table to Able, and Food as Medicine.

Image Credit: Grempz / Flickr

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Is it Better to Bake, Boil, or Steam Sweet Potatoes?

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I previously talked about the cancer fighting properties of sweet potatoes (See Anti-Cancer Potential of Sweet Potato Proteins) and what would happen if you centered your diet around them (The Okinawa Diet: Living to 100). It seems that the only potential downside to eating too many sweet potatoes is that you could get yellow palms (or nose as you can see in the video, The Best Way to Cook Sweet Potatoes), a harmless condition called "carotenemia." Caused by elevated levels of beta carotene in the blood, it was first noticed a century ago when carrots were introduce into infant diets. It's treated mostly by just reassuring parents that it's harmless, but if we don't want our child's nose to be yellow, we can decrease their beta carotene intake and in a few months it will be gone.

When picking out varieties at the supermarket, the intensity of the yellow or orange flesh color of the sweet potato is directly correlated to its nutritional content, so the more intense the better. Though if you really want intensity, sweet potato varieties don't just range from white to yellow and orange, but from pink to deep purple. The natural pigments that cause these colors may have special anticancer effects.

What is the best way to cook sweet potatoes? Boiling may actually retain most of the antioxidant power of sweet potatoes, compared to roasting and steaming. If we compare baking to boiling microscopically, boiling helps thin out the cell walls and gelatinize the starch, which may enhance the bioavailability of nutrients. At the same time, the glycemic index of boiled sweet potatoes was found to be about half that of baking or roasting, so boiled sweet potatoes give us less of a blood sugar spike.

Make sure to keep the skin on, though. The peel of a sweet potato has nearly ten times the antioxidant power as the flesh (an antioxidant capacity comparable to that of blueberries). However, the peel's nutrition really takes a hit when baked, which wipes out over two thirds of the antioxidants, whereas microwaving or boiling are comparatively much gentler. The same is true for the rest of the sweet potato. Baking can also cause an 80% drop in vitamin A levels, twice as much as boiling. Therefore, from a nutritional standpoint, boiling rather than baking should be recommended for cooking sweet potato.

Boiling may theoretically be best, but sweet potatoes are so incredibly healthy that the actual best way to prepare them is whichever way will get you to eat the most of them! The exception is deep frying, which can lead to the formation of acrylamide, a potential human carcinogen.

What about cooking methods for other vegetables? See my video Best Cooking Method.

Want more information about acrylamide, the potential crispy carb carcinogen? See my video Cancer Risk from French Fries. And for why deep frying in general might not be good, Deep Frying Toxins and Carcinogens in the Smell of Frying Bacon.

-Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death, More Than an Apple a Day, From Table to Able, and Food as Medicine.

Image Credit: Avital Pinnick / Flickr

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